FINAL Flashcards
Gastroesophageal Reflux Disease (GERD) Patho
Weak, lower esophageal sphincter tone allows reflux of acid pepsin into esophagus
Risk Factors for GERD
- Age
- High BMI
- Smoking
- Large meals
- Acidic foods, caffeine, alcohol
Causes of Peptic Ulcer Disease (PUD)
- H. Pylori bacteria (bacterial infection in stomach)
- Alcohol
- NSAIDs (non-steroidal anti-inflamm drugs)
- Smoking
- Medications
Diverticulitis Patho
Infected diverticulum pouch = inflammation
CMs of Diverticulitis
- Cramping & abdominal pain (in LLQ)
- Diarrhea, constipation, distention, flatulence
- Fever, leukocytosis
- N/V
- Diverticular hemorrhage: melena (dark stools from blood), rectal bleeding
Diverticulosis vs Diverticulitis
-litis = inflammed pouches; infection
-losis = development of abnormal pouches; asymptomatic
Ulcerative Colitis
- Chronic ulceration
- Affects inner most lining (mucosa) of the large colon & rectum
- Continuous; no skipped lesions
- Stools = bloody & mucous
- Abdominal cramping
- Incrd risk for colon cancer
Crohn’s Disease
- Chronic, relapsing
- Can affect any part of GI tract from mouth to anus of the entire thickness
- Discontinuous; skipped lesions
- Cobblestone appearance
- Abdominal pain
- Diarrhea w/ or w/out blood
- Anemia from malabsorption
Complications of Lower GI Disorders
- Fistula: abnormal opening/pathway of 2 surfaces tht aren’t suppose to touch
- Abscess: collection of infection under skin
- Perforation w/ peritonitis: a hole tht develops in wall of organ tht becomes inflammed
- Necrotic bowel
Portal Hypertension Patho
Localized pressure in portal veins (of liver) is high due to scarring of the liver causing blood to not go back to heart resulting in accumulation of blood = HTN
(high BP in portal venous system; >10mmHg)
CM for Portal HTN
- Esophageal varices
- Ascites
- Splenomegaly
- Hepatic Encephalopathy
Cirrhosis Patho
- End stage liver disease
- Functional liver replaced by fibrosis & scarring
- Constrictive bands disrupt flow of blood vessels & biliary ducts
>leads to portal HTN bc blood is not metabolize
>leads to bile stasis from obstruction of biliary channels = death of liver cells & liver failure
Causes of Cirrhosis
- Alcohol
- Viral hepatitis
- Autoimmune
- Primary & secondary biliary cirrhosis (destructive of bile ducts)
- Nonalcoholic fatty liver disease
Causes of Jaundice
- Excessive destruction of RBCs
- Impaired uptake of bilirubin by liver cells
- Drcd conjugation of bilirubin
- Obstruction of bile flow
- Excessive extrahepatic production of bilirubin
(basically cirrhosis?)
Jaundice Patho
Fibrotic liver cells are unable to uptake bilirubin, metabolize bilirubin, and excrete bilirubin in bile
Hepatitis Prevention
- Hep A: hand-washing (fectal-oral route)
- Hep C: avoid shared needles & blood of someone else infected
(most common reason for liver transplant)
Hepatitis CMs + Phases
- Prodromal / Pre-icterus
>abrupt to insidious: malaise, myalgia, fatigue, anorexia, N/V, diarrhea, abdominal pain, fever chills; serum lvls of AST & ALT incr - Icterus (jaudice); 7-14 days laters
>jaundice, pruritus, liver tenderness, rise in serum bilirubin - Recovery; complete recovery 1-4 mnths
>jaundice disappears, return to normal
Lab Values of Liver Dysfunction
- Liver enzymes: high
>aspartate transaminase (AST): highest in hepatitis/cancers
>alanine transaminase (ALT): specific to liver inflamm
>alkaline phosphatase (ALP): liver disease; bile obstruction - Bilirubin: high
- Prothrombin Time (bleeding): prolonged; liver isn’s synthesizing clotting factors & vit K
- Ammonia: high
- Albumin: low
Substances of Gallstones
- Cholesterol
- Biliary salts
Causes of Cholecystitis
- Calculous (90%): obstruction by stones = inflammation
- Acalculous (10%): infection/sepsis or trauma; no stones
Pancreatitis Patho
- Autodigestion (pancreas digesting itself) of tissue by abnormal activation of pancreatic enzymes (trypsin)
- Inflammatory response
- Incrd vascular permeability leads to hemorrhage, edema, & necrosis
>mild to severe symptoms
>may progress to multi-organ failure
Why NPO for Pancreatitis
Signal to pancreas to produce enzymes is not activated
Type I Diabetes
- No insulin secretion
- Autoimmune/idiopathic
- Destruction of beta-cells
- Cannot modify risk
- Peak age: 12-14yrs
- DKA if CM not caught in time
- CM: polyuria, polydipsia, polyphagia
Type II Diabetes
- Some functional insulin
- Defect insulin receptors
- Incrd insulin resistance
- Can modify some risk to prevent or delay onset
- Peak age > 40yrs
- Complications at diagnosis
- CMs: 3 Ps, blurred vision/retinopathy, paresthesia/PVD, fatigue, frequent infections, wounds slow healing, candida (yeast) infections